Ambien and a bump to the head with surprising consequences

A 42 year old female was in good health until she took an Ambien one night to help with some insomnia. Apparently she got up during sleep (sleep walking), went into the kitchen, and began to cook a meal. She then proceeded to fall down and bang her head. She presented to my office with a headache, some dizziness and severe pain and swelling in her lower extremities. Her calf muscles were extremely swollen and tender. I was concerned that she might have a subdural hematoma ( a clot in the skull) or rhabdomyolysis, a condition of muscle breakdown after injury which can lead to kidney failure. I sent her to the ER for a work up. The results were negative.

She came back in a day later. Her calf muscles were increasingly tight, swollen and painful. I was worried about a DVT (a blood clot). I sent her for a duplex (ultrasound) study to exclude this. It was negative. The pain was increasing in intensity. Narcotics, at a fairly high dose were needed to control the pain. The Percocet was not working; she returned with tears streaming down her face. She did not have myositis--inflammation of the muscles because the muscle enzyme CPK or CK was normal. Did she has some sort of myopathy? I ran some blood tests for an autoimmune disease. Oddly, her rheumatoid factor was elevated at 285. New symptoms appeared: there was now a tremor of her arms. I started a tapering dose of steroids. It was of no help.

A neurological exam was performed. Deep tendon reflexes were absent across the board. Pin prick sensation was decreased in a stocking/glove pattern affecting all limbs. Vibratory sensation was minimal in the feet. A tick borne disease panel was ordered.

The results: Lyme ELISA IgM 0.91--equivocal range, Lyme WB 41 IgM and IgG bands, Babesia WA1 antibody elevated 1:256, C6 peptide 0.2, CD57 63. Did she in fact have tick borne illness? Had trauma activated a latent tick borne infection leading to an autoimmune syndrome with progressive symptoms in a previously well individual? That was my thinking.

And her symptoms were progressive--rapidly. She developed uncontrolled rhythmic seizure like jerking of her arms. This was associated with uncontrolled vocalizations typical of Tourettes syndrome. The pain and muscle swelling continued to be severe and difficult to manage. She developed night sweats. None of these symptoms existed prior to her traumatic injury.

Treatment for Lyme and Babesia with typical antimicrobials over a 2 month period has been successful. The neuro symptoms--the seizures and Tourettes resolved. The pain and swelling has lessened. She is now returning to work half time, a feat which would have been unimaginable a few weeks ago.

This is the clinical vingette.

These are my thoughts--conjectures.

There are a large number of patients who harbor Lyme (Bb) and its associated co-infections without clinical illness. These parasitic entities are contained by the host and its immune system.
The healthy state can be quite tenuous. Many things can unleash the ticking bomb: intercurrent infection, stress or even physical trauma.

The percent of individuals in endemic areas who are assymptomatic carriers of TBD may be much higher than suspected, given my suspicion that the vast majority of infected individuals exhibit no symptoms of disease.

A positive Lyme ELISA test should not be discounted when the second tier--the Western Blot is negative. Any positive result for Lyme: ELISA, Western Blot or C6 peptide should be considered as potential evidence of the disease.

Positive tests for Babesia WA1 or Babesia duncani have become extremely common, much more so than B. microti. There has to date been no acknowledgement of this change in distribution of this parasite from the west coast to the east coast by health departments.

There are better sleeping medications than Ambien.